Vitamin K Administration in Elderly Stroke Patients with Sepsis and Elevated INR
Direct Answer
Yes, intravenous vitamin K should be administered to elderly stroke patients presenting with sepsis and deranged INR, using 10 mg IV by slow infusion over 30 minutes, with repeat INR measurement at 12-24 hours to distinguish vitamin K deficiency from hepatic synthetic dysfunction. 1
Clinical Context and Rationale
The combination of sepsis and elevated INR in an elderly stroke patient creates a complex clinical scenario requiring careful assessment:
- Sepsis-induced coagulopathy commonly presents with isolated prolonged INR that may reflect true vitamin K deficiency (from poor nutrition, antibiotic therapy, or malabsorption) rather than pure hepatic synthetic dysfunction 1
- Elderly patients with stroke history have amplified bleeding risk at any given INR level, making correction of coagulopathy particularly important 2, 3
- The key diagnostic question is whether the elevated INR represents correctable vitamin K deficiency versus irreversible liver failure 1
Diagnostic Approach: Distinguishing Vitamin K Deficiency from Liver Failure
Therapeutic Trial Protocol
Administer 10 mg vitamin K intravenously by slow infusion and reassess INR after 12-24 hours: 1
- INR improvement ≥0.5 within 24-72 hours confirms vitamin K deficiency as a significant component 1
- Persistently elevated INR indicates hepatic synthetic dysfunction predominates 1
Laboratory Patterns to Guide Decision-Making
Vitamin K deficiency pattern: 1
- Prolonged PT/INR with normal or near-normal fibrinogen (>150 mg/dL)
- All vitamin K-dependent factors low (II, VII, IX, X)
- Non-vitamin K-dependent factors relatively preserved
Hepatic synthetic dysfunction pattern: 1
- Prolonged PT/INR with low fibrinogen (<100-150 mg/dL)
- Both vitamin K-dependent AND non-vitamin K-dependent factors low
- Often accompanied by thrombocytopenia and elevated von Willebrand factor
Dosing and Administration Protocol
Standard Dosing for Septic Patients
Dose: 10 mg vitamin K (maximum; do not exceed this dose) 2, 1
Route: Intravenous, administered as slow infusion over 30 minutes to minimize anaphylactoid reactions 2, 1, 3
Monitoring schedule: 1
- Recheck INR at 12-24 hours after administration
- If INR remains abnormal, monitor every 6-8 hours for the next 24-48 hours
- A minority of patients may require additional vitamin K doses over the following week
Special Considerations for Sepsis
- Cholestatic liver disease (jaundice, elevated bilirubin) in septic patients warrants parenteral vitamin K before attributing coagulopathy to other causes, with repeat INR obtained within 2-5 days 1
- Antibiotic therapy in sepsis commonly depletes vitamin K stores, making deficiency more likely 1
- Poor nutrition and malabsorption in critically ill septic patients increase the probability of true vitamin K deficiency 1
Critical Safety Considerations
Anaphylactoid Reaction Risk
- Incidence: 3 per 100,000 IV doses via non-IgE mechanism, likely due to polyoxyethylated castor oil solubilizer 2, 3
- Manifestations: Cardiac arrest, severe hypotension, bradycardia/tachycardia, dyspnea, bronchospasm 2, 3
- Prevention: Always administer by slow IV infusion over 30 minutes, never as IV push 2, 1
Dosing Caveats
Never exceed 10 mg vitamin K: 2, 3
- Higher doses create a prothrombotic state
- Prevent re-anticoagulation for days if warfarin needs to be restarted
- May complicate management if therapeutic anticoagulation becomes necessary
When Vitamin K Alone Is Insufficient
Indications for Prothrombin Complex Concentrate (PCC)
If the patient has active life-threatening bleeding in addition to elevated INR: 2, 3
- Administer 4-factor PCC 25-50 U/kg IV plus vitamin K 10 mg IV simultaneously
- PCC achieves INR correction within 5-15 minutes versus hours with vitamin K alone
- Vitamin K must still be given to stimulate endogenous production of vitamin K-dependent factors and prevent "rebound" anticoagulation
Dosing Algorithm for PCC (if needed):
Important: PCC carries thrombotic risk; thromboprophylaxis must be considered as early as possible after bleeding control 2, 3
What NOT to Do
Avoid These Common Pitfalls
- Do not use subcutaneous vitamin K in septic patients—it does not modify coagulation parameters effectively in liver disease 2, 1
- Do not routinely correct elevated INR with vitamin K in the absence of bleeding or vitamin K deficiency in patients with chronic liver disease—it is ineffective and not evidence-based 2, 1
- Do not use fresh frozen plasma (FFP) as first-line therapy for vitamin K deficiency—it requires large volumes, carries risk of transfusion-associated circulatory overload, and does not address the underlying deficiency 2
- Do not assume all elevated INR in sepsis represents liver failure—therapeutic trial with vitamin K is essential to identify correctable deficiency 1
Expected Response and Follow-Up
Timeline for INR Correction
- Vitamin K begins working within 4-6 hours when given intravenously 2
- Partial correction typically seen at 12 hours 4
- Maximal effect achieved at 24 hours 5, 4
- If no improvement by 24 hours, hepatic synthetic dysfunction is the primary problem 1
Interpretation of Response
Good response (INR drops ≥0.5): 1
- Confirms vitamin K deficiency component
- May require additional vitamin K doses if INR remains elevated
- Address underlying causes (antibiotics, malnutrition, malabsorption)
Poor response (INR remains elevated): 1
- Indicates severe hepatic synthetic dysfunction
- Vitamin K will not be effective
- Consider targeted blood product replacement only if active bleeding occurs
- Avoid volume overload from excessive FFP transfusions
Management of Underlying Sepsis
While correcting the INR, simultaneously address:
- Source control of sepsis
- Antibiotic therapy (recognizing this may worsen vitamin K deficiency)
- Nutritional support to prevent further vitamin K depletion
- Monitoring for bleeding complications given the patient's stroke history and elderly age
The decision to administer vitamin K in this clinical scenario is both diagnostic and therapeutic, providing critical information about the nature of the coagulopathy while potentially correcting a reversible deficiency.